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Hypercalciuric rickets: metabolic studies and pathophysiological considerations.

M Tieder, R Samuel, U A Liberman

    Nephron
    |January 1, 1985
    PubMed
    Summary
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    Childhood idiopathic hypercalciuria with rickets is caused by a primary renal phosphate leak. Oral phosphorus treatment accelerated growth and cured rickets by correcting phosphate depletion.

    Area of Science:

    • Pediatric Endocrinology
    • Nephrology
    • Metabolic Bone Disease

    Background:

    • Childhood idiopathic hypercalciuria is a rare condition presenting with dwarfism, renal tubular abnormalities, and bone lesions.
    • Metabolic studies are crucial for understanding complex pediatric endocrine and renal disorders.

    Observation:

    • The patient exhibited hyperphosphaturia, hypophosphatemia, hypercalciuria with normocalcemia, and elevated 1,25-dihydroxycholecalciferol (1,25(OH)2D3).
    • Intestinal calcium and phosphorus hyperabsorption, low parathyroid hormone (PTH), and low urinary adenosine 3':5'-cyclic monophosphate (c-AMP) were noted.
    • Bone biopsy confirmed rickets, consistent with phosphate depletion.

    Findings:

    • A primary renal phosphate leak leads to hypophosphatemia, stimulating 1,25(OH)2D3 synthesis.

    Related Experiment Videos

  • Enhanced intestinal calcium absorption suppresses PTH and c-AMP, resulting in secondary hypercalciuria.
  • Phosphate depletion is the primary cause of rickets in this condition.

    • Implications:

    • Understanding the pathophysiological sequence is key to managing this rare disorder.
    • Oral phosphorus supplementation effectively treats rickets and normalizes calcium excretion in affected children.
    • This case highlights the intricate relationship between phosphate, vitamin D, and calcium metabolism in pediatric bone health.